Naloxone suppresses ischemic arrhythmias via potentiating baroreflex
Abstract
AIM: To study the relationship between the anti-arrhythmia action of naloxone (Nal) and its effect on baroreflex sensitivity (BRS).
METHODS: Acute myocardial infarction was produced by ligating coronary artery in Sprague-Dawley rats. Ventricular extrasystole (VE), tachycardia (VT), and fibrillation (VF) were recorded on ECG. The slopes of linear regression (b) from systolic blood pressure and cardiac cycle after intravenous injection (i.v.) of phenylephrine 2 micrograms was taken as the BRS. The area of infarct was estimated after TTC staining.
RESULTS: Nal 0.5 mg i.v., intracisternal injection (i.c.) of Nal 0.1 mg, and i.c. beta-endorphin (beta-End) antiserum 10 microL suppressed the ischemic arrhythmias, arrhythmia score was 1.8 +/- 1.1 (Nal i.v.) vs 3.8 +/- 2.1 (Saline i.v.); 1.7 +/- 1.5 (Nal i.c.) vs 4.0 +/- 2.6 (Artificial CSF i.c.) and 1.7 +/- 1.6 (beta-End antiserum i.c.) vs 4.1 +/- 2.0 (Serum i.c.) (P < 0.05) and potentiated the BRS, BRS was 4.2 +/- 1.8 (Nal i.v.) vs 2.9 +/- 0.8 (saline i.v.); 4.5 +/- 1.7 (Nal i.c.) vs 2.8 +/- 0.7 (Artificial CSF i.c.) and 4.4 +/- 1.1 (beta-End antiserum i.c.) vs 3.0 +/- 0.9 (Serum i.c.) (P < 0.05). BRS showed negative relations to the arrhythmia scores with r of -0.69 for i.v Nal, -0.72 for i.c. Nal, and -0.67 for i.c. beta-End antiserum (P < 0.05).
CONCLUSION: Nal suppressed ischemic arrhythmias via antagonization of beta-endorphin and potentiation of BRS.
Keywords:
METHODS: Acute myocardial infarction was produced by ligating coronary artery in Sprague-Dawley rats. Ventricular extrasystole (VE), tachycardia (VT), and fibrillation (VF) were recorded on ECG. The slopes of linear regression (b) from systolic blood pressure and cardiac cycle after intravenous injection (i.v.) of phenylephrine 2 micrograms was taken as the BRS. The area of infarct was estimated after TTC staining.
RESULTS: Nal 0.5 mg i.v., intracisternal injection (i.c.) of Nal 0.1 mg, and i.c. beta-endorphin (beta-End) antiserum 10 microL suppressed the ischemic arrhythmias, arrhythmia score was 1.8 +/- 1.1 (Nal i.v.) vs 3.8 +/- 2.1 (Saline i.v.); 1.7 +/- 1.5 (Nal i.c.) vs 4.0 +/- 2.6 (Artificial CSF i.c.) and 1.7 +/- 1.6 (beta-End antiserum i.c.) vs 4.1 +/- 2.0 (Serum i.c.) (P < 0.05) and potentiated the BRS, BRS was 4.2 +/- 1.8 (Nal i.v.) vs 2.9 +/- 0.8 (saline i.v.); 4.5 +/- 1.7 (Nal i.c.) vs 2.8 +/- 0.7 (Artificial CSF i.c.) and 4.4 +/- 1.1 (beta-End antiserum i.c.) vs 3.0 +/- 0.9 (Serum i.c.) (P < 0.05). BRS showed negative relations to the arrhythmia scores with r of -0.69 for i.v Nal, -0.72 for i.c. Nal, and -0.67 for i.c. beta-End antiserum (P < 0.05).
CONCLUSION: Nal suppressed ischemic arrhythmias via antagonization of beta-endorphin and potentiation of BRS.